Increased urine albumin is associated with atherosclerotic disease and
predicts cardiovascular morbidity and mortality in nondiabetic popula
tions. This finding is frequently postulated to reflect the impact of
atherosclerotic damage on glomerular and systemic capillary permeabili
ty, an interesting but as yet untested hypothesis. The transcapillary
escape rate of albumin (TERalb, the 1-hour decline rate of intravenous
I-125-albumin, a measure of capillary macromolecular permeability), a
lbuminuria, lipid levels, echocardiographic wall thickness, and insuli
n responses to oral glucose were measured in 30 untreated dipstick-neg
ative lean men and clinically stable atherosclerotic peripheral vascul
ar disease; tolerance to oral glucose was a requirement for inclusion
in the study. Because hypertension per se might influence TERalb, the
sample included either normotensive (n=18, 118+/-6/72+/-7 mm Hg) or hy
pertensive (n=12, 141+/-7/84+/-6 mm Hg by 24-hour blood pressure monit
oring) arteriopathic patients; 11 normal age- and gender-matched subje
cts (121+/-7/76+/-5 mm Hg) were used as control subjects. TERalb was h
igher in patients (10.7+/-3.2 versus 7.4+/-1.7%/h, P<0.013), a differe
nce that persisted after postload glucose, insulin, and lipid levels w
ere accounted for by covariance analysis; atherosclerosis and hyperten
sion together did not further impair vascular permeation to albumin. I
n contrast with TERalb, albuminuria was elevated only in the hypertens
ive subgroup; the 2 variables showed no relationship, even when the da
ta were analyzed separately in normotensive and hypertensive subgroups
. Urine albumin correlated positively with 24-hour blood pressure and
wall thickness. Thus, systemic capillary permeability is altered in no
ndiabetic atherosclerotic patients independently from blood pressure l
evels, but this abnormality is not reflected by proportionate changes
in albuminuria.